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Research Article
Livio Provenzi
Fondazione Istituto Neurologico Nazionale Casimiro Mondino
Corresponding Author
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The COVID-19 pandemic represents a collective trauma that may have enduring stress effects during sensitive periods, such as pregnancy. Prenatal stress may result in epigenetic signatures of stress-related genes (e.g., the serotonin transporter gene, SLC6A4) that may in turn influence infants’ behavioral development. In April 2020, we launched a longitudinal cohort study to assess the behavioral and epigenetic vestiges of COVID-19-related prenatal stress exposure in mothers and infants. COVID-19-related prenatal stress was retrospectively assessed at birth. SLC6A4 methylation was assessed in thirteen CpG sites in mothers and infants’ buccal cells. Infants’ temperament was assessed at 3-month-age. Complete data were available from 108 mother-infant dyads. Greater COVID-19-related prenatal stress was significantly associated with higher infants’ SLC6A4 methylation in seven CpG sites. SLC6A4 methylation at these sites predicted infants’ temperament at 3 months. Clinicians and policymakers should promote timely preventive actions to promote infant well-being during and after the present pandemic.
Keywords
COVID-19, DNA methylation, infants, epigenetics, pandemic, pregnancy, prenatal stress, SLC6A4, temperament
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No competing interests reported.
This is a list of supplementary files associated with this preprint. Click to download.
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View the published article at Scientific Reports.
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Posted 12 May, 2021
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See the published version of this preprint at Scientific Reports.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Livio Provenzi
Fondazione Istituto Neurologico Nazionale Casimiro Mondino
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Scientific Reports.
Version 1
Posted 12 May, 2021
No community comments so far
Editorial decision: Major revision
On 11 Jun, 2021
Reviews received
Received 28 May, 2021
Reviewers agreed
On 17 May, 2021
Reviewers invited
Invitations sent on 17 May, 2021
Editor assigned
On 17 May, 2021
Editor invited
On 17 May, 2021
Submission checks complete
On 07 May, 2021
First submitted
On 03 May, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Scientific Reports.
The COVID-19 pandemic represents a collective trauma that may have enduring stress effects during sensitive periods, such as pregnancy. Prenatal stress may result in epigenetic signatures of stress-related genes (e.g., the serotonin transporter gene, SLC6A4) that may in turn influence infants’ behavioral development. In April 2020, we launched a longitudinal cohort study to assess the behavioral and epigenetic vestiges of COVID-19-related prenatal stress exposure in mothers and infants. COVID-19-related prenatal stress was retrospectively assessed at birth. SLC6A4 methylation was assessed in thirteen CpG sites in mothers and infants’ buccal cells. Infants’ temperament was assessed at 3-month-age. Complete data were available from 108 mother-infant dyads. Greater COVID-19-related prenatal stress was significantly associated with higher infants’ SLC6A4 methylation in seven CpG sites. SLC6A4 methylation at these sites predicted infants’ temperament at 3 months. Clinicians and policymakers should promote timely preventive actions to promote infant well-being during and after the present pandemic.
Figure 1
Figure 2
Figure 3
Figure 4
No competing interests reported.
This is a list of supplementary files associated with this preprint. Click to download.
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